Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.
Genomics Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA.
Microbiology (Reading). 2010 Apr;156(Pt 4):1120-1133. doi: 10.1099/mic.0.032896-0. Epub 2009 Dec 24.
Salmonella invade non-phagocytic cells by inducing massive actin rearrangements, resulting in membrane ruffle formation and phagocytosis of the bacteria. This process is mediated by a cohort of effector proteins translocated into the host cell by type III secretion system 1, which is encoded by genes in the Salmonella pathogenicity island (SPI) 1 regulon. This network is precisely regulated and must be induced outside of host cells. In vitro invasive Salmonella are prepared by growth in synthetic media although the details vary. Here, we show that culture conditions affect the frequency, and therefore invasion efficiency, of SPI1-induced bacteria and also can affect the ability of Salmonella to adapt to its intracellular niche following invasion. Aerobically grown late-exponential-phase bacteria were more invasive and this was associated with a greater frequency of SPI1-induced, motile bacteria, as revealed by single-cell analysis of gene expression. Culture conditions also affected the ability of Salmonella to adapt to the intracellular environment, since they caused marked differences in intracellular replication. These findings show that induction of SPI1 under different pre-invasion growth conditions can affect the ability of Salmonella to interact with eukaryotic host cells.
沙门氏菌通过诱导大量肌动蛋白重排来侵入非吞噬细胞,导致膜皱襞形成和细菌的吞噬作用。这个过程由一群效应蛋白介导,它们通过 III 型分泌系统 1 被转运到宿主细胞中,III 型分泌系统 1 由沙门氏菌致病性岛(SPI)1 调控子中的基因编码。这个网络受到精确的调控,必须在宿主细胞外诱导。尽管细节有所不同,但在体外侵袭性沙门氏菌是通过在合成培养基中生长来制备的。在这里,我们表明培养条件会影响 SPI1 诱导细菌的频率,从而影响入侵效率,并且还可以影响沙门氏菌在入侵后适应其细胞内小生境的能力。好氧生长的晚期指数期细菌的侵袭性更强,这与通过单细胞基因表达分析揭示的 SPI1 诱导的运动细菌的更高频率有关。培养条件还影响了沙门氏菌适应细胞内环境的能力,因为它们导致细胞内复制的明显差异。这些发现表明,在不同的入侵前生长条件下诱导 SPI1 可以影响沙门氏菌与真核宿主细胞相互作用的能力。